Fourteen of eighteen aged adults studied had impared B cell colony growth which appeared secondary to intrinsic B cell defects and/or impared monocyte (MO) accessory cell function. Previous reports from our laboratories and others have well characterized normal human B cell colony responses and have shown that colony formation can potentially yield valuable insights into aberrant human immunoregulation undetectable in conventional liquid cultures. The first phase of these studies will investigate the nature of intrinsic B cell and MO aberrancies which might be responsible for diminished colony growth of aged B cells stimulated by Staph protein A (SpA). In young adults, most colony precursors are functionally mature and express high densities of surface immunoglobulin (sIg) and Ia like antigens (sIa). We will therefore examine by cytofluorometry if the diminished colony responses of aged adults are secondary to a loss of these mature populations. Because interleukin 1 (IL-1) is extremely important in MO accessory cell function supporting colony growth, we will determine if the diminished accessory cell function of aged MO represents an impairment in basal and stimulated IL-1 production. The second series of experiments will investigate if aged humans have imbalances within OKT regulator or autohelper activity which can alter normal B cell colony growth. These experiments will also evaluate if aged B cell colony precursors are responsive to young OKT regulation and young autohelper activity. Should aberrant T cell regulation of colony growth be found in aged humans then we will determine if these abnormalities represent deficient IL-1 promotion of IL-2 production or an intrinsic inability of aged T cells to elaborate IL-2. These experiments should be capable of detecting previously undefined aberrancies within the aged B cell system. Also, these studies will evaluate the role of interleukins in aged humans and therefore could provide a possible basis for future therapeutic applications.